Post-traumatic stress disorder, emotional processing and Inappropriate Implantable Cardioverter-Defibrillator Shocks: clinical consideration by a single case report = Disturbo post-traumatico da stress, profilo cognitivo-emotivo e shocks inappropriati del defibrillatore cardiaco impiantabile: Considerazioni cliniche attraverso un single case report

Introduction. Even though an overwhelming amount of evidence supports the clinical efficacy and safety of the implantable cardioverter defibrillator (ICD), inappropriate shocks for atrial arrhythmias with rapid ventricular conduction or for abnormal sensing results in multiple adverse effects Presentation. In this study we present the case of a 59- year-old woman who was admitted to hospital for ICD implantation with a past medical history that was positive for non-ischemic dilated cardiomyopathy, congestive heart failure (NYHA class III), atrial fibrillation, essential hypertension and a recent episode of syncope. Since in the 18 months follow-up the patient suffered many inappropriate shocks, we investigated the association of the presence of a PTSD (Post- Traumatic-Stress-Disorder) prior to implantation and a specific profile of cognitive processing emotions, with the effectiveness of the ICD. Emotional distress states and cognitive thoughts preceding ICD shock inappropriate episode were recorded by structured mobile diary (eMotional-ICDiary). We outlined how the presence of a highly traumatic event which had occurred 6 years previously was related to a recurrence of a combination of moderate distress and cognitive thoughts, associated with episodes of Inappropriate Shock. A psycho-diagnostic examination and the administration of the Emotional Processing Scale (EPS-25) and Emotional Regulation Questionnaire (ERQ) outlined that the patient presented a profile of cognitive processing of emotions characterized by elevated levels of unprocessed emotions, low appraisal and high suppression emotional regulation strategy. Conclusion. The observations gathered in this single case are a good starting point for further research in order to check if the post-traumatic stress disorder and a specific cognitive profile connected to the processing of emotions are associated with the presence of inappropriate ICD shocks. Further larger sample studies are required in this area

Development of the designed ankyrin repeat protein (DARPin) G3 for HER2 molecular imaging

s funded by the Seventh Framework Programme (FP7) for HER Imaging and Molecular Interaction Mapping in Breast Cancer (Imagint EC grant 259881) and the Breast Cancer Campaign. The research was supported by the National Institute for Health Research University College London Hospitals Biomedical Research Centre

Decreased Fatty Acid Transporter FABP1 and Increased Isoprostanes and Neuroprostanes in the Human Term Placenta: Implications for Inflammation and Birth Weight in Maternal Pre-Gestational Obesity.

The rise in prevalence of obesity in women of reproductive age in developed and developing countries might propagate intergenerational cycles of detrimental effects on metabolic health. Placental lipid metabolism is disrupted by maternal obesity, which possibly affects the life-long health of the offspring. Here, we investigated placental lipid metabolism in women with pre-gestational obesity as a sole pregnancy complication and compared it to placental responses of lean women. Open profile and targeted lipidomics were used to assess placental lipids and oxidised products of docosahexaenoic (DHA) and arachidonic acid (AA), respectively, neuroprostanes and isoprostanes. Despite no overall signs of lipid accumulation, DHA and AA levels in placentas from obese women were, respectively, 2.2 and 2.5 times higher than those from lean women. Additionally, a 2-fold increase in DHA-derived neuroprostanes and a 1.7-fold increase in AA-derived isoprostanes were seen in the obese group. These changes correlated with a 70% decrease in placental FABP1 protein. Multivariate analyses suggested that neuroprostanes and isoprostanes are associated with maternal and placental inflammation and with birth weight. These results might shed light on the molecular mechanisms associated with altered placental fatty acid metabolism in maternal pre-gestational obesity, placing these oxidised fatty acids as novel mediators of placental function

The HANDE-QMC Project: Open-Source Stochastic Quantum Chemistry from the Ground State Up.

Building on the success of Quantum Monte Carlo techniques such as diffusion Monte Carlo, alternative stochastic approaches to solve electronic structure problems have emerged over the past decade. The full configuration interaction quantum Monte Carlo (FCIQMC) method allows one to systematically approach the exact solution of such problems, for cases where very high accuracy is desired. The introduction of FCIQMC has subsequently led to the development of coupled cluster Monte Carlo (CCMC) and density matrix quantum Monte Carlo (DMQMC), allowing stochastic sampling of the coupled cluster wave function and the exact thermal density matrix, respectively. In this Article, we describe the HANDE-QMC code, an open-source implementation of FCIQMC, CCMC and DMQMC, including initiator and semistochastic adaptations. We describe our code and demonstrate its use on three example systems; a molecule (nitric oxide), a model solid (the uniform electron gas), and a real solid (diamond). An illustrative tutorial is also included

Long non-coding RNA PCAT19 safeguards DNA in quiescent endothelial cells by preventing uncontrolled phosphorylation of replication protein A2

In healthy vessels, endothelial cells maintain a stable, differentiated, and growth-arrested phenotype for years. Upon injury, a rapid phenotypic switch facilitates proliferation to restore tissue perfusion. Here we report the identification of the endothelial cell-enriched long non-coding RNA (lncRNA) PCAT19, which contributes to the proliferative switch and acts as a safeguard for the endothelial genome. PCAT19 is enriched in confluent, quiescent endothelial cells and binds to the full replication protein A (RPA) complex in a DNA damage- and cell-cycle-related manner. Our results suggest that PCAT19 limits the phosphorylation of RPA2, primarily on the serine 33 (S33) residue, and thereby facilitates an appropriate DNA damage response while slowing cell cycle progression. Reduction in PCAT19 levels in response to either loss of cell contacts or knockdown promotes endothelial proliferation and angiogenesis. Collectively, PCAT19 acts as a dynamic guardian of the endothelial genome and facilitates rapid switching from quiescence to proliferation